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. Author manuscript; available in PMC: 2022 Feb 1.
Published in final edited form as: J Mol Cell Cardiol. 2020 Oct 29;151:56–71. doi: 10.1016/j.yjmcc.2020.10.012

Figure 3. Structural substrates of human AF.

Figure 3.

A. Evaluation of atrial fibrosis by histology and LGE-MRI. Left to right: Fibrosis is upregulated in association with AF in comparison to patients with no history of AF by histology. In-vivo studies showed that the extent of atrial fibrosis was a significant predictor of ablation failure, and likelihood of AF reentrant mechanism increases in areas of high enhancement. Adapted from Platonov et al.2011 [152]; Marrouche et al. 2017 [10, 172]; Cochet et al. 2018 [12]. B. Arrhythmogenic 3D structural substrates in AF driver maintenance. From left to right: Reentrant AF driver identified optically overlapped with 3D CE-MRI anatomy. Bi-atrial wall thickness variations, transmural 3D fibrosis distribution (sub-epi (blue), mid-wall (green), and sub-endo (red)) as well as 3D myofiber tracts created arrhythmogenic hubs for reentrant AF drivers. Adapted from Zhao et al 2017 [113]. C. Histological validation improves ex-vivo and in-vivo fibrosis MRI analysis. Ex-vivo 3D CE-MRI reconstruction shows fibrosis in red and myofibers in blue. In-vivo 3D CE-MRI shows fibrosis islands in possible driver regions. Adapted from Hansen et al. 2015, 2017 [8, 77]; Csepe et al. 2017 [180]. Abbreviations AF – atrial fibrillation; LGE-MRI – late gadolinium enhanced magnetic resonance imaging; IVC/SVC –inferior and superior vena cava; LA/RA – left and right atria; LAA –left atrial appendage; LIPV/LSPV/RIPV/RSPV – left, right, superior, inferior pulmonary veins; CE-MRI – contrast enhanced magnetic resonance imaging; PLA –posterior left atrium